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J Neurosci. 2016 Jun 1;36(22):5914-9. doi: 10.1523/JNEUROSCI.0051-16.2016.

Visual Deprivation During the Critical Period Enhances Layer 2/3 GABAergic Inhibition in Mouse V1.

Author information

1
Department of Neuroscience, Program in Cellular Neuroscience, Neurodegeneration, and Repair, Yale University School of Medicine, New Haven, Connecticut 06510, and.
2
Department of Biology, University of Southern California, Los Angeles, California 90089.
3
Department of Neuroscience, Program in Cellular Neuroscience, Neurodegeneration, and Repair, Yale University School of Medicine, New Haven, Connecticut 06510, and m.higley@yale.edu.

Abstract

The role of GABAergic signaling in establishing a critical period for experience in visual cortex is well understood. However, the effects of early experience on GABAergic synapses themselves are less clear. Here, we show that monocular deprivation (MD) during the adolescent critical period produces marked enhancement of GABAergic signaling in layer 2/3 of mouse monocular visual cortex. This enhancement coincides with a weakening of glutamatergic inputs, resulting in a significant reduction in the ratio of excitation to inhibition. The potentiation of GABAergic transmission arises from both an increased number of inhibitory synapses and an enhancement of presynaptic GABA release from parvalbumin- and somatostatin-expressing interneurons. Our results suggest that augmented GABAergic inhibition contributes to the experience-dependent regulation of visual function.

SIGNIFICANCE STATEMENT:

Visual experience shapes the synaptic organization of cortical circuits in the mouse brain. Here, we show that monocular visual deprivation enhances GABAergic synaptic inhibition in primary visual cortex. This enhancement is mediated by an increase in both the number of postsynaptic GABAergic synapses and the probability of presynaptic GABA release. Our results suggest a contributing mechanism to altered visual responses after deprivation.

KEYWORDS:

gephyrin; interneuron; monocular deprivation; optogenetics

PMID:
27251614
PMCID:
PMC4887562
DOI:
10.1523/JNEUROSCI.0051-16.2016
[Indexed for MEDLINE]
Free PMC Article
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